My Body My Story

Racial Discrimination & Cardiovascular Disease Risk: My
Body My Story Study of 1005 US-Born Black and White

Community Health Center Participants (US)
Nancy Krieger
1
*, Pamela D. Waterman
1
, Anna Kosheleva
1
, Jarvis T. Chen
1
, Kevin W. Smith
2
,
Dana R. Carney
3
, Gary G. Bennett
4
, David R. Williams
1,5
, Gisele Thornhill
6
, Elmer R. Freeman
6
1Department of Social and Behavioral Sciences, Harvard School of Public Health, Boston, Massachusetts, United States of America, 2Senior Data Analyst, RTI International
Waltham, Massachusetts, United States of America, 3Haas School of Business, University of California, Berkeley, California, United States of America, 4Psychology and
Neuroscience and Duke Global Health Initiative, Duke University, Durham, North Carolina, United States of America, 5Professor, Department of Sociology, Harvard
University, Cambridge, Massachusetts, United States of America, 6Center for Community Health Education Research and Service, Boston, Massachusetts, United States of
America
Abstract
Objectives: To date, limited and inconsistent evidence exists regarding racial discrimination and risk of cardiovascular
disease (CVD).
Methods: Cross-sectional observational study of 1005 US-born non-Hispanic black (n =504) and white (n =501) participants
age 3564 randomly selected from community health centers in Boston, MA (20082010; 82.4% response rate), using 3
racial discrimination measures: explicit self-report; implicit association test (IAT, a time reaction test for self and group as
target vs. perpetrator of discrimination); and structural (Jim Crow status of state of birth, i.e. legal racial discrimination prior
1964).
Results: Black and white participants both had adverse cardiovascular and socioeconomic profiles, with black participants
most highly exposed to racial discrimination. Positive crude associations among black participants occurred for Jim Crow
birthplace and hypertension (odds ratio (OR) 1.92, 95% confidence interval (CI) 1.28, 2.89) and for explicit self-report and the
Framingham 10 year CVD risk score (beta =0.04; 95% CI 0.01, 0.07); among white participants, only negative crude
associations existed (for IAT for self, for lower systolic blood pressure (SBP; beta =24.86; 95% CI 29.08, 20.64) and lower
Framingham CVD score (beta =20.36, 95% CI 20.63, 20.08)). All of these associations were attenuated and all but the
white IAT-Framingham risk score association were rendered null in analyses that controlled for lifetime socioeconomic
position and additional covariates. Controlling for racial discrimination, socioeconomic position, and other covariates did
not attenuate the crude black excess risk for SBP and hypertension and left unaffected the null excess risk for the
Framingham CVD score.
Conclusion: Despite worse exposures among the black participants, racial discrimination and socioeconomic position were
not associated, in multivariable analyses, with risk of CVD. We interpret results in relation to constrained variability of
exposures and outcomes and discuss implications for valid research on social determinants of health.
Citation: Krieger N, Waterman PD, Kosheleva A, Chen JT, Smith KW, et al. (2013) Racial Discrimination & Cardiovascular Disease Risk: My Body My Story Study of
1005 US-Born Black and White Community Health Center Participants (US). PLoS ONE 8(10): e77174. doi:10.1371/journal.pone.0077174
Editor: Andrea S. Wiley, Indiana University, United States of America
Received February 1, 2013; Accepted August 30, 2013; Published October 18, 2013
Copyright: 2013 Krieger et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits
unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: The study was funded by the National Institutes of Health/National Institute on Aging (1 R01 AG027122-01 and R01AG27122-3S1); the funder had no
role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing Interests: The authors have declared that no competing interests exist.
* E-mail: nkrieger@hsph.harvard.edu
Introduction
Although research on self-reported exposure to racial discrim-
ination and health has documented consistent positive associations
between higher exposure and adverse mental health, studies on
somatic diseases and their risk factors are less conclusive, and have
reported both positive and null findings [13], including for risk
factors for cardiovascular disease (CVD), the most commonly
studied somatic outcome [16]. To address these discrepancies,
new work is emphasizing the need for improved measurement of
exposure to racial discrimination, at multiple levels, from
individual to structural, as experienced across the lifecourse and
historical generation [1,2,7,8]. Also garnering concern is the
sociodemographic composition of study participants, given
evidence that: (a) experiences and reporting of racial discrimina-
tion and its health impact may vary by lifetime socioeconomic
position and nativity, and (b) ceiling and floor effects may
constrain testing hypotheses, whereby if experiences of racial
discrimination or of poverty are uniformly high in a given set of
study participants, there may be insufficient variation to observe
the postulated associations [1,5,7,9,10].
PLOS ONE | www.plosone.org 1 October 2013 | Volume 8 | Issue 10 | e77174
We accordingly designed the My Body My Story (MBMS) [11] to:
(1) use a range of racial discrimination measures spanning from
individual to structural, childhood to the present-day, and explicit
self-report to implicit assessment using timed reaction tests, and (2)
examine their associations with risk of chronic disease in a sample
of US-born black and white Americans ranging from impover-
ished to economically secure. In this paper, we focus on risk of
CVD, analyzed in relation to 3 outcomes: systolic blood pressure
(SBP), hypertension, and the Framingham 10-year CVD risk
score, an integrated measure that incorporates data on age,
diabetes, smoking, treated and untreated blood pressure, total
cholesterol, HDL cholesterol, and body mass index (BMI) [12,13].
Guiding our study design and analytic plan, from choice of
hypotheses and study participants to selection and modeling of
exposure, outcome, and covariates, is the ecosocial theory of
disease distribution, which is focused on how people literally
embody their societal and ecological context, at multiple levels and
across the lifecourse and historical generations, thereby producing
population patterns of health, including health inequities [1416].
Specifically, in the case of racism and health, ecosocial theory
conceptualizes racial/ethnic health inequities as biological expres-
sions of racism and posits that there are many pathways, not just
one, by which racism can harm health, with relevant pathways
shaped by historical context [1,7,17]. These pathways can include:
(a) economic and social deprivation; (b) excess exposure to toxins,
hazards, and pathogens; (c) social trauma; (d) health-harming
responses to discrimination; (e) targeted marketing of harmful
commodities; (f) inadequate medical care; and (g) especially (but
not only) for Indigenous peoples, ecosystem degradation and
alienation from the land [1,7,17]. Additional core constructs
pertain to: (1) the interplay of exposure, susceptibility, and
resistance (individually and collectively), and (2) issues of account-
ability (causal responsibility for) and agency (the power and ability
to act) at every level; a corollary is that peoples bodies can tell
stories that they may be unable or unwilling to articulate regarding
the impact of racial discrimination upon their lives, including on
their health [1,7,11,18]. As ecosocial theory emphasizes, it is
impossible for any given study to attempt to measure every
specified pathway at every level and at all relevant spatiotemporal
scales. Rather, the value of a theoretical framework is that it can
help concretize systematic substantive thinking about potential
causal pathways, how the selected constructs and entities are
operationalized and measured, the types of statistical analyses
conducted, potential threats to validity, and the complexities
involved in interpreting study findings [7,16,19].
We accordingly used 3 approaches to measure racial discrim-
ination, as follows.
(1) Explicit self-report (Figure 1), using two of the most widely-
used and validated instruments [1,2,7,20]: the Experiences of
Discrimination (EOD) measure [21,22] and the Everyday
Discrimination Scale (EDS (any) for any unfair treatment, and
Figure 1. Measures of racial discrimination: implicit and explicit.
doi:10.1371/journal.pone.0077174.g001
Racial Discrimination & Cardiovascular Disease
EDS (race) for unfair treatment attributed to race/ethnicity)
[23]. Both instruments measure both lifetime and recent
exposure, but employ different approaches to obtaining data
(EOD: 1-part question; EDS: 2 part question, first about
experiences of unfair treatment, followed by question about
attributing why, e.g., to race); of note, research has shown
that these non-equivalent approaches to obtaining data result
in different estimates of exposure and association with health
outcomes [1,7,24].
(2) Implicit Association Test (IAT) (Figure 1), a time-reaction test
that measures unconscious associations, free from bias due to
social concerns affecting self-report data [25]. For the implicit
approach, we used a novel IAT we have formulated
[11,26,27], the first to measure whether people unconsciously
associate themselves and also their racial/ethnic group with
being a target versus perpetrator of discrimination.
(3) Structural, referring to population-level exposures that can
shape but are not reducible to interpersonal interactions and
individual experiences [1,7]. To assess one aspect of structural
discrimination, we used a new measure of Jim Crow
birthplace status (i.e., born in a US state with legal racial
discrimination abolished by the 1964 US Civil Rights Act)
[1,7,28], a variable which simultaneously links levels (i.e., state
and individual), lifecourse, and historical generation [1,7].
Table 1. My Body My Story study participants sociodemographic and socioeconomic characteristics: 504 black and 501 white
community health center members, all US-born, non-Hispanic, ages 3564 (Boston, MA, 20082010).
Variable
Observed data Missing: N (%)
Black White Black White
Age (mean (SD)) years 48.6 (8.0) 49.0 (8.0) 0 0
Gender (%) women 69.2 63.1 0 0
Poverty: (% US poverty line) (%) below poverty line 33.8 21.3 63 (12.5) 36 (7.2)
.100 and ,200% 21.8 18.5
.=200 and ,400% 19.1 19.1
.=400% 25.4 41.1
Education (%) less than high school 16.1 9.9 0 4 (0.8)
.= high school but ,4 yrs college 68.5 56.5
.=4 yrs college 15.5 33.6
Occupational class (%) owner/self-employed/supervisor 20.9 34.6 1 (0.2) 4 (0.8)
non-supervisory employee 36.2 29.0
unemployed/not in paid labor force/other 42.9 36.4
Wealth (other than home) (%) no financial assets 78.7 54.2 72 (14.3) 40 (8.0)
any financial assets 21.3 45.8
high financial assets (.=$5,000) 7.2 30.6 88 (17.5) 63 (12.6)
Household received public
assistance (%)
as a child 52.8 33.2 50 (9.9) 25 (5.0)
in the last year 43.6 28.6 18 (3.6) 8 (1.6)
Housing tenure (%) rent for cash 68.2 46.6 26 (5.2) 12 (2.4)
paying mortgage/own home 26.4 48.6
reside without paying rent cash 5.4 4.7
Census tract poverty (20052009) (%) ,5% below poverty 6.8 18.5 18 (3.6) 36 (7.2)
59% below poverty 8.4 27.1
1019% below poverty 32.1 30.5
.=20 below poverty (poverty area) 52.7 25.8
Parent/guardian born in US (%): mother/female guardian 94.8 91.2 1 (0.2) 2 (0.4)
father/male guardian 93.7 90.5 11 (2.2) 7 (1.4)
Parents/guardians education:
highest attained by either
parent/guardian (%):
less than high school 27.3 12.0 83 (16.5) 33 (6.7)
.= high school but ,4 yrs college 55.1 51.3
.=4 yrs college 17.6 36.8
Parents/guardians education:
at most high school degree or GED
(general equivalence diploma (%):
mother/female guardian 70.5 61.3 90 (17.9) 39 (7.8)
father/male guardian 72.0 54.9 136 (27.0) 64 (12.8)
Note: outcomes in bold font have values that differ significantly (p,0.05) comparing the black versus white study participants.
doi:10.1371/journal.pone.0077174.t001
Our a priori hypotheses were that: (a) each measure of exposure
of racial discrimination (explicit; implicit; structural) would be
associated, with increased risk of CVD, albeit not necessarily to the
same extent, since each captures different aspects of exposure
[1,2,7,9,25]; and (b) controlling for all 3 types of exposure to racial
discrimination, along with diverse measures of socioeconomic
position, would attenuate any observed black/white differences in
risk of CVD, per the hypothesized pathways of embodiment
leading from discrimination to health inequities involving social
trauma and economic deprivation [1,7,1618].
Materials and Methods
As described previously [11], we recruited the 1005 MBMS
participants (504 black, 501 white) from a random sample of the
membership rosters of four community health centers in Boston,
MA; enrollment extended from August 2008 through December
2010, a period encompassing the economic downturn linked to the
20072008 collapse of the US housing market and subsequent
bank failures in 2008. The sample size was based on power
analyses regarding likely prevalence of exposure and expected
increased risk (as documented in the literature at the time of
planning the study in 2007), which indicated we would have at
least 80% power to detect hypothesized effect sizes $0.3 for high
versus low exposure to racial discrimination for the specified
health outcomes [11].
Ethics statement
The study protocol, implemented in accordance with the
Helsinki Declaration of 1975, as revised in 2000, was approved by
the Harvard School of Public Health Office of Human Research
Administration (protocol #11950127, which covered 3 of the 4
health centers through reciprocal IRB agreements), and was also
separately approved by the fourth community health centers
Institutional Review Board. All participants provided written
informed consent. To ensure protection of the study participants
confidentiality, the informed consent document stipulated that no
data from the study may be shared without the consent of the
study participants, the directors of the four community health
centers from which they were recruited, and also the studys
principal investigator.
Study participants
To be eligible, persons had to self-report they were US-born,
non-Hispanic, age 35 to 64, and self-identify as black or white (the
preferred approach to classifying race/ethnicity for health research
[1,2,7,9]). Fully 94.4% of eligible screened persons agreed to
participate (black: 97.0%; white: 91.9%). The overall response
rate, defined as: (completed interviews)/eligible [29], equaled
82.4% (black: 86.0%; white: 81.4%) [11]. We interviewed
participants at the health centers and obtained the racial
discrimination, demographic, socioeconomic, psychosocial, an-
thropometric, biological, health status and health behavior data
listed in Tables 1, 2, and 3 in five ways:
(1) Audio-Computer Assisted Self-Interviewing (ACASI) [30],
for the survey, administered on a computer laptop;
(2) the IAT [11,26,27] (Figure 1), also administered on the
laptop, with order counterbalanced with the ACASI survey
(whereby participants were randomly assigned to complete the
ACASI first, followed by the IAT, versus the IAT first, followed
by the ACASI, in order to avoid order effects, e.g., response to
IAT influenced by having taken the ACASI first, or response to
ACASI influenced by having taken the IAT first);
(3) a finger stick, to obtain blood for automated on-site analysis
of the CVD biomarkers, using the validated Cholestech LDX
instrument [31];
(4) a physical exam, for the anthropometric [32] and blood
pressure [33] data; and
(5) geocoding of residential address to link to census-tract
poverty level [34].
The final step of the study protocol was to debrief the
participants and give them a $75 grocery card and a 26-page
resource booklet (6
th
grade literacy level) which included: (1) a two-
page study debriefing statement, which briefly described the
purpose of the study and the way the IAT performs as a sorting
task, (2) information on their blood pressure, body measurements,
and CVD biomarkers, plus text to help interpret these data and
provide guidance to keep levels healthy, and (3) a resource section
on organizations that provide legal assistance to address racial
discrimination, and also mental health and social services [11].
Study variables: exposures, outcomes, and covariates
In our prior methodological paper reporting on the racial
discrimination, sociodemographic, and psychosocial variables
[11], we provide detailed descriptions of the validated instru-
ments employed to obtain these data. Here we briefly present the
measures used, delineate how we obtained the health outcome
data, and describe methods for obtaining other covariates as
warranted.
Exposures: racial discrimination. (1) EOD [21,22]
(Figure 1). The continuous EOD measure ranged from 0 to 9
(the number of domains in which racial discrimination were ever
experienced, specified in response to a 1-stage question asking
about experiences of discrimination), with data also obtained on
frequency of occurrence [22]. The categorical measure used cut-
points based on prior research and classified participants as self-
reporting no (0 domains), moderate (12 domains), or high (3+
domains) exposure [21,22]. Data on response to unfair treatment
was obtained using 2 yes/no questions, resulting in a 4-category
typology: take action/talk to others; take action/keep quiet; accept
as fact of life/talk to others; accept as fact of life/keep quiet
[21,22]. Additional questions (Figure 1) pertained to worry about
racial discrimination against oneself and ones racial/ethnic group,
both as a child and in the last year [22].
(2) EDS. [22,23,35] (Figure 1). Data were based on the short
version of the EDS [35], which is a 2-part question, the first of
which asks about everyday experiences of unfair treatment in 5
domains (EDS (any); scored 05) and their typical frequency, the
second of which asks for attribution of reasons for these
experiences, with 9 options provided (all of which could be
checked). Persons who selected race or ancestry and national
origin were classified as having experienced unfair treatment due
to race/ethnicity, i.e., racial discrimination (EDS (race)).
(3) IAT (Figure 1). The two IATs were reaction-time tests
regarding the associations of, respectively, self vs others, and black
vs white, as target vs perpetrator of racial discrimination
[11,26,27]. We analyzed each IAT as a continuous variable and
in the analytic models also included an interaction term, to allow
for synergistic effects (beyond additive) between sense of self and
sense of racial/ethnic group as target vs perpetrator of racial
discrimination.
(4) Jim Crow state of birth. Participants were classified as having
been born in a Jim Crow state if they were born in any of the 21
states plus the District of Columbia that had legal racial
discrimination overturned by the 1964 US Civil Rights Act; the
21 states were: Alabama, Arizona, Arkansas, Delaware, Florida,
Georgia, Kansas, Kentucky, Louisiana, Maryland, Mississippi,
Missouri, New Mexico, North Carolina, Oklahoma, South
Carolina, Tennessee, Texas, Virginia, West Virginia, and
Wyoming [7,11,28].
Cardiovascular outcomes. To obtain valid cardiovascular
data, we asked all participants to fast for at least 8 hours prior to
the exam, and all multivariable analyses controlled for whether
participants had followed these instructions and also whether
Table 2. My Body My Story study participants exposure to racial discrimination and psychosocial characteristics: 504 black and 501
white community health center members, all US-born, non-Hispanic, ages 3564 (Boston, MA, 20082010).
Variable
Exposure to racial discrimination
Explicit (self-report)
Experiences of Discrimination
[EOD; racial discrimination
only]: ever (lifetime)
2 (0.4) 1 (0.2)
continuous (mean (SD)) number of domains or situations
(range: 09)
3.8 (2.7) 1.2 (1.7)
categorical (%) 0 situations 14.1 50.2
12 situations 21.7 32.2
3+ situations 64.1 17.6
Everyday discrimination (EDS):
in day-to-day life exposed at
least 1x/year
9 (1.8) 4 (0.8)
EDS (any): continuous (mean (SD)) (range: 05) 2.5 (1.6) 2.2 (1.5)
categorical (%) unfair treatment .=1x/yr 86.3 85.1
EDS (race): continuous for
unfair treatment due to
race (mean (SD))
(range: 05) 1.8 (1.8) 0.5 (1.3)
categorical (%) unfair treatment due to
race .=1x/yr
59.2 18.5
Worried about racial
discrimination (%)
as a child, against self 70.2 20.2 1 (0.2) 2 (0.4)
as a child, against own racial/
ethnic group
69.8 30.1 1 (0.2) 2 (0.4)
in last year, against self 64.0 20.8 1 (0.2) 2 (0.4)
in last year, against own racial/
ethnic group
71.8 31.5 1 (0.2) 2 (0.4)
Implicit
IAT effect (mean, SD) total Black vs White (de-trended and
centered on w/b/t/m) (IAT B/W)
0.26 (0.32) 0.13 (0.39) 10 (2.0) 10 (2.0)
total Me vs Them (de-trended
and centered
onw/b/t/m) (IAT M/T)
0.24 (0.36) 0.19 (0.34) 11 (2.2) 10 (2.0)
Structural
Jim Crow birthplace status (%) born in Jim Crow state 30.2 5.8 0 1 (0.2)
Psychosocial measures
Response to unfair treatment (%) take action and talk to
others (act/talk)
68.2 64.3 1 (0.2) 0
take action and keep
to self (act/quiet)
9.3 10.0
accept as fact of life and
talk to others
(accept/talk)
14.7 16.4
accept as fact of life and
keep to self (accept/quiet)
7.8 9.4
Social desirability (mean (SD)) (range: 0100) 43.8 (31.7) 28.2 (29.5) 27 (5.4) 11 (2.2)
they had consumed food or alcohol or had smoked cigarettes
8 hours before the exam.
(1) SBP. We computed the average blood pressure based on 3
readings, taken 1 minute apart, obtained after participants had
watched a 3-minute relaxation video, and as measured using a
validated automatic blood pressure monitor (Omron HEM-
711AC) [33].
Table 3. My Body My Story study participants health-related characteristics: 504 black and 501 white community health center
members, all US-born, non-Hispanic, ages 3564 (Boston, MA, 20082010).
Variable
Anthropometric
Height (cm) (mean (SD)) 167.9 (8.5) 168.3 (9.0) 0 3 (0.6)
Weight (kg) (mean (SD)) 91.2 (22.6) 83.3 (21.4) 0 2 (0.4)
Body mass index (BMI; kg/m
2
)
(mean(SD))
32.4 (8.0) 29.3 (6.9) 0 3 (0.6)
Obese (BMI .=30) (%) 57.1 39.4 0 3 (0.6)
Waist circumference (cm)
(mean (SD))
a
104.3 (15.9) 100.0 (16.0) 0 4 (0.8)
Hip circumference (cm)
(mean (SD))
a
113.0 (16.4) 106.0 (15.1) 0 4 (0.8)
Waist-to-hip ratio 0.92 (0.07) 0.94 (0.07) 0 4 (0.8)
Behavioral
Smoking (%) current smoker 43.8 34.5 0 0
ex-smoker 16.9 34.5
never smoker 39.3 30.9
Physical activity (International
Physical Activity
Questionnaire [IPAQ]) (%)
low 28.4 21.2 1 (0.2) 0
moderate 30.6 38.3
high 41.0 40.5
Sleep: usual hours
on weekdays/
workdays (%)
7 or more hours 22.8 35.1 0 0
5 to 7 hours 63.1 53.9
,5 hours 14.1 11.0
Cardiovascular disease outcomes and related health variables
Blood pressure: mm Hg (mean (SD))
b
systolic 131.6 (16.0) 125.3 (16.1) 6 (1.2) 4 (0.8)
diastolic 83.4 (10.7) 79.4 (10.4) 6 (1.2) 4 (0.8)
Hypertension (%) yes 62.5 41.4 8 (1.6) 6 (1.2)
Cholesterol: mg/dL (mean (SD))
b
Total 175.9 (35.1) 185.8 (36.9) 7 (1.4) 13 (2.6)
LDL 103.0 (32.2) 112.6 (33.1) 58 (11.5) 69 (13.8)
HDL 49.4 (16.0) 49.0 (16.6) 23 (4.6) 19 (3.8)
Total/HDL cholesterol ratio 3.9 (1.6) 4.2 (1.7) 27 (5.4) 23 (4.6)
Triglycerides: mg/dL (mean (SD))
b
130.9 (84.9) 140.2 (94.9) 33 (6.5) 47 (9.4)
CVD history (self-report) (%) yes 11.1 9.6 0 0
Diabetes (%) yes 25.2 15.1 4 (0.8) 12 (2.4)
Framingham cardiovascular
disease (CVD)
10 year risk
score (mean (SD))
everyone 10.9 (10.2) 9.6 (9.2) 47 (9.3) 45 (9.0)
only persons with no
self-reported
CVD history
10.1 (9.4) 9.1 (9.1) 41 (9.2) 38 (8.4)
a
% measured over clothes: (a) waist: black =86.1%; white =73.5%; (b) hip: black =95.6%; white =93.2%.
b
Values for blood pressure, cholesterol, and triglycerides are reported as measured, regardless of participants use of medication for these outcomes or their fasting
status.
(2) Hypertension (HBP). We defined hypertension as per the
guidelines of the 7
th
Joint National Committee on Prevention,
Detection, Evaluation, and Treatment of High Blood Pressure
[36], i.e., measured systolic blood pressure .=140 mm Hg OR
measured diastolic blood pressure .=90 mm Hg OR taking
blood pressure medication, with this medication history ascer-
tained using validated questions employed in the National Health
and Nutrition Examination Survey (NHANES) [37].
(3) Framingham CVD 10-year risk score [12]. We computed
this score, which predicts risk (expressed as a percent) of
developing cardiovascular disease in the next 10 years among
persons free of CVD [12]. We ascertained if persons were free of
CVD using the validated NHANES questions pertaining to
history of CVD, referring to whether the person reported ever
having been diagnosed with congestive heart failure, coronary
heart disease, angina, heart attack, or stroke [37]. To create the
Framingham CVD risk score, we used the gender-specific
equations that incorporate data on the following variables: age,
diabetes, smoking, treated and untreated blood pressure, total
cholesterol, HDL cholesterol, body mass index (BMI) [12]. We
obtained data on each component of the score (above and beyond
blood pressure and HBP medication, described above) as follows:
(a) Age. Self-report.
(b) Diabetes. We followed the American Diabetes Association
guidelines [38] and categorized participants as diabetic if either
(i) their fasting glucose was .=126 mg/dL, or (i) their fasting
glucose was ,126 mg/dL and they either were taking medicine
for diabetes or self-reported having been told by a physician that
they had diabetes.
(c) Smoking. In addition to asking if participants had smoked in
the 8 hours prior to the exam, we also employed validated
questions to determine smoking status (current, ex, never) used
in the National Health Interview Survey (NHIS) [39].
(d) Cholesterol (total and HDL). We employed the validated
Cholestech LDX instrument [31] to obtain an on-site assay of
cholesterol levels, along with data on triglyceride levels.
(e) BMI. Following NHANES protocols [32], we measured:
standing height with a stadiometer (with shoes removed) to the
nearest 0.635 cm (J inch) and weight with an electronic scale,
to the nearest 0.09 kg (0.2 pounds).
Additional covariates. We obtained additional data on
diverse sociodemographic, economic, psychosocial, anthropomet-
ric, and health behavior covariates relevant to testing the study
hypotheses. In our analytic models, we retained only those
variables that were associated with the exposure or outcome in at
least one racial/ethnic group. Below we list the covariates we
considered for analysis that did and did not meet our inclusion
criteria for the analytic models; all were measured using
validated instruments that are detailed in our prior methodolog-
ical MBMS paper and prior analyses [11,22].
(a) Sociodemographic. (i) Included: Age; gender; (ii) Not
included: relationship status; parents nativity; and racial/
ethnic composition of neighborhood.
(b) Socioeconomic. (i) Included: poverty level; educational level
(participant; participants parents/guardians); census tract
poverty; (ii) Not included: household income; occupational
class; debt; wealth; receipt of public assistance; and housing
tenure.
(c) Psychosocial. (i) Included: social desirability [40]; (ii) Not
included: racial/ethnic centrality score [41]; hostility
[42,43], and occurrence of serious life event in the last year
[44].
(d) Anthropometric. Included: waist and hip circumference with
a circumference tape, to the nearest mm [32], and used to
compute the waist-to-hip ratio; (ii) Not included: tibia length,
measured with a flexible cloth tape, to the nearest 0.635 cm
(J inch) [32].
(e) Health behavior. (i) Included: smoking (component of the
Framingham risk score; see above [39]); (ii) Not included:
physical activity [45]; average number of hours of sleep per
night [46].
In Tables 1, 2, and 3 we report descriptive data on all retained
covariates and also selected covariates not included in the analytic
model that nonetheless provide relevant descriptive data about the
study participants and their context.
Statistical analyses
We conducted all analyses in SAS [47]. Guided by our
theoretical framework, we assessed bivariate associations between
the 3 cardiovascular outcomes (SBP; hypertension; Framingham
10-year CVD risk scores) and our a priori specified exposures and
covariates and then retained in the analytic models only those
variables empirically demonstrating statistically significant associ-
ations (p,0.05) in at least one racial/ethnic group for at least one
outcome. We analyzed the Framingham risk score as an outcome,
rather than its particular components (except for systolic blood
pressure), because this clinically-relevant score provides a more
physiologically and empirically integrated measure of cardiovas-
cular risk than any one item by itself [12,13]. Because analyses
modeling the EOD as a categorical variable (0, 12, 3+) yielded no
evidence of non-linear effects, we report only results for the
continuous measure. We did not include the EDS (for any or
race) in the analytic models because neither measure was
associated with any of the outcomes.
To address the modest level of missing data (typically under 5%,
except for the socioeconomic variables; see Tables 1, 2, and 3), we
implemented multiple imputation via the Amelia II program [48]
to create 5 imputed data sets. The imputation model included all
variables retained for the analytic models (with imputations
performed on component items for composite variables and re-
combined in each data set), and we combined estimates across the
imputed data sets using standard methods. We used linear and
logistic regression, respectively, for the continuous and dichoto-
mous outcomes; we analyzed the Framingham risk score on the
log scale due to skewed distribution. We first conducted analyses
separately for the black and white participants and then conducted
analyses based on all participants to compare the black versus
white risk of the outcome.
Results
Study participant profile: sociodemographic
composition, exposure to racial discrimination, and
health characteristics
Sociodemographic composition (Table 1). All participants
were, by design, US-born, and the parents/guardians of over 90%
of the black and white participants were also US-born. Both the
black and white participants had adverse economic profiles, but
the black participants, as previously reported [11], nevertheless
were ,1.5 times more likely to experience socioeconomic
deprivation (p,0.05). For example, 33.8% of black and 21.3%
of white participants were below the US poverty line; 53.7% and
23.8% respectively lived in census tracts with .=20% below
poverty (i.e., a level reaching the US census definition of poverty
area [34]); and 84.5% and 66.4% had ,4 yrs college. Despite
being working age (range: 3564; mean: 49 y), a high proportion
of the black (42.9%) and white (36.4%) participants were not in the
paid labor force. Moreover, only 26.4% of the black, compared to
48.6% of the white, participants were either paying mortgage on
or owned their home outright, and 78.7% versus 54.2%,
respectively, had no financial assets other than their home.
Attesting to economic adversity across the lifecourse, over half the
black participants (52.8%) and one-third of the white participants
(33.2%) reported their household had received public assistance
when they were a child, proportions slightly higher than those for
currently receiving public assistance (43.6% and 28.6% respec-
tively), and the highest educational level attained by their parents/
guardians was, for the majority of the black and white participants,
at most a high school diploma or GED (general equivalence
diploma).
Racial discrimination (Table 2). As also previously report-
ed [11], the black compared to white participants were 2 to
3 times more likely (p,0. 05) to be exposed to racial discrimina-
tion (implicit, explicit, and structural). For example, fully 64.1% of
the black participants, as compared to 17.6% of the white
participants, reported having ever experienced racial discrimina-
tion in 3 or more domains, 70.2% v. 20.2% worried about being a
target of racial discrimination as a child, and 30.2% vs. 5.8% were
born in a Jim Crow state. Black compared to white participants
also scored significantly higher on both IAT tests for being more
likely to associate themselves and their racial/ethnic group as
being a target vs. perpetrator of racial discrimination (IAT me vs
them: 0.24 vs. 0.19; IAT black vs white: 0.26 vs. 0.13). Among
both groups, as expected [26,27] and also previously reported
[11], the weak correlation (r,0.10) between the explicit and
implicit measures was non-significant (p.0.05). Black and white
participants, moreover, exhibited similar responses to unfair
treatment, with 68.2% and 64.3%, respectively, taking action
and talking to others, and only 7.8% and 9.4% accepting it as a
fact of life and keeping it to themselves. Notably, and as previously
reported [11], social desirability scores were 1.5 times higher
(p,0.05) among the black compared to white participants (43.8 vs.
28.2).
Health outcomes (Table 3). The black compared to white
participants were significantly more likely (p,0.05), by 1.1 to
1.6 times, to have a generally poorer health profile, including for
the Framingham 10-year CVD risk score (overall and also among
persons free of CVD) and most of its components (BMI, systolic
and diastolic blood pressure, current smoking, treated and
untreated hypertension) and also for waist and hip circumference,
obesity, low physical activity, and inadequate sleep. Their profiles
were similar, however, for HDL cholesterol and self-reported
histories of CVD, and significantly better (p,0.05) for waist-to-hip
ratio, total and LDL cholesterol, and total/HDL cholesterol ratio.
Overall, 57.1% of the black participants and 39.4% of the white
participants were obese, 62.5% and 41.4% were hypertensive,
their mean SBP (for all persons, whether or not taking anti-
hypertensive medication) respectively equaled 131.6 and
125.3 mm Hg, and among persons free of CVD, their risk of
developing CVD in the next 10 years was, respectively, 10.1% and
9.1%.
Analytic results (statistical models)
Among the racial discrimination measures, statistically signifi-
cant positive crude associations (95% CI excluded 0 for betas from
the linear regression models and 1 for the odds ratio from the
logistic regression models) occurred, among black participants
only, between: (1) the Jim Crow measure and hypertension,
uncontrolled hypertension, and the two Framingham scores
(Table 4 and Table 5) and (2) the EOD and the Framingham
CVD risk score (Table 5). Among the white participants only, a
statistically significant inverse crude association occurred between
the IAT me vs. them and both SBP and the Framingham CVD
risk score (Table 4 and Table 5). Additionally, with regard to the
socioeconomic variables, statistically significant crude positive
associations for hypertension (Table 4) and Framingham CVD risk
score (Table 5) existed with low parental/guardian education
(black participants) and low participant education (both black and
white participants). A crude positive association also tended to
exist, for black participants, between poverty and hypertension.
In the multivariable models (Table 4 and Table 5; see Table S1
for parameter estimates for the additional variables controlled for
in the analyses), the sole racial discrimination measure among
black participants that displayed a statistically significant associ-
ation occurred in the analyses for uncontrolled hypertension,
whereby the odds ratio (OR) for the IAT for me vs. them
(comparing risk for persons more vs. less likely to associate
themselves personally, versus others, as being a target of racial
discrimination) equaled 2.85 (95% confidence interval (CI) 1.05,
7.75). In these multivariable models, none of the measures of
socioeconomic position remained significant among the black
participants.
Among white participants, only one measure of racial discrim-
ination exhibited any association with any of the health outcomes:
the IAT me vs them, which showed a weak inverse association
with the Framingham 10-year CVD risk score (b on the log scale:
20.17, 95% CI 20.33, 20.01) (Table 5). The sole socioeconomic
measure that exhibited any statistically significant association was
participants education, whereby risk was slightly elevated for the
Framingham CVD risk score among persons who had at least a
high school education but less than 4 years of college, as compared
to persons with 4 years of college or more (Table 5).
Lastly, regarding the extent to which control for racial
discrimination and socioeconomic position attenuated the ob-
served crude black excess risk for the 3 study outcomes (SBP,
hypertension, Framingham CVD risk score), results indicated that,
first, following adjustment for age and gender, the black/white
differences remained statistically significant for only two outcomes
(Table 6, Model 1): SBP (average excess: 3.79 mm Hg, 95% CI
1.81, 5.76) and hypertension (odds ratio: 2.40, 95% CI, 1.77,
3.24). Additional control for racial discrimination (Model 2) and
socioeconomic position (Model 3), separately or together (Model
4), each in conjunction with other core covariates, did not
eliminate the black excess risk for either SBP or hypertension.
Discussion
Our central findings were that within a random sample of
working age US-born black and white American members of 4
urban health centers who overall had a poor socioeconomic and
cardiovascular health profile, black participants were more likely
than white participants (p,0.05) to be impoverished (33.8% vs.
21.3%), to self-report exposure to racial discrimination (in 3 or
more situations: 64.1% vs 17.6%, including as a child: 70.2% vs
20.2%), to associate their racial/ethnic group and themselves with
being a target vs perpetrator of racial discrimination (IAT effect:
0.26 vs. 0.13 and 0.24 vs. 0.19, respectively), and to have been
born in a Jim Crow state (30.2% vs. 5.8%). Nevertheless, despite
markedly higher levels of exposure to racial discrimination and
impoverishment among the black compared to white participants,
crude associations of racial discrimination and risk of CVD among
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the black participants were not robust to control for socioeconomic
position and other covariates, nor did controlling for exposure to
racial discrimination and socioeconomic adversity account for the
black excess risk for elevated SBP and risk of hypertension or affect
the null excess risk (after controlling for age and gender) for the
Framingham CVD score.
Study limitations and strengths: considering the MBMS
participants in context
As a first step in interpreting our study findings, it is important
to consider study limitations and strengths. One limitation is that
our investigation, by virtue of study design, was cross-sectional,
limiting causal inference, even as we did obtain data on exposure
to racial discrimination and socioeconomic position across the
lifecourse. Strengths include: the high response rate within our
random sample; little missing data; and reliance on both validated
instruments and innovative use of new implicit and structural
racial discrimination measures.
A second limitation pertains to the unexpectedly poor and
constrained socioeconomic and health profile of both the black
and white participants. Here we note that we chose to recruit
participants from community health centers [11] for two
important reasons. First, the mandate of community health
centers is to provide health care to persons who are low income
and medically underserved, as well as are diverse in their racial/
ethnic composition [49], and so are likely to serve populations who
are harmed by racial discrimination and economic deprivation.
Second, community health centers are trusted community-based
organizations [49], which is especially important for recruiting
participants from social groups that have been subjected to social
and economic deprivation and historically exposed to unethical
research practices [50]; the high MBMS participation (black:
97.0%; white: 91.9%) and response rates (black: 86.0%; white:
81.4%) attest to the value of this recruitment strategy [11]. A
corollary is that community health centers are used by individuals
who value these aspects of community health centers, whether or
not low income, thereby resulting in an economically heteroge-
neous (and not solely low income) membership [49].
Thus, as expected, the MBMS study participants both black and
white, spanned from those with lower to higher income and
education, whereby although 33.8% of the black and 21.3% of the
white participants were below the US poverty line and 16.1% and
Table 5. Univariate and multivariable associations of racial discrimination and socioeconomic position with Framingham 10-year
cardiovascular risk scores: My Body My Story study (504 black, 501 white US born non-Hispanic participants; Boston, 20092010)
(imputed data).
Variable
Framingham CVD 10-yr risk score (log-transformed values)
b (95% CI)
Black White
Univariate Multivariable Univariate Multivariable
Racial discrimination
Explicit
EOD: continuous (09) 0.04 (0.01, 0.07) 20.01 (20.03, 0.01) 0.03 (20.02, 0.08) 0.00 (20.03, 0.03)
Implicit
IAT: black vs. white (B/W) as target 20.09 (20.38, 0.20) 20.17 (20.38, 0.05) 20.02 (20.26, 0.21) 20.01 (20.17, 0.14)
IAT: me vs. them (M/T) as target 20.20 (20.45, 0.06) 20.03 (20.24, 0.19) 20.36 (20.63, 20.08) 20.17 (20.33, 20.01)
Interaction: IAT B/W x IAT M/T 0.15 (20.35, 0.65) 20.13 (20.52, 0.27)
Structural
born in Jim Crow state: yes vs. no (ref) 0.57 (0.38, 0.76) 20.08 (20.22, 0.06) 20.08 (20.49, 0.33) 0.22 (20.01, 0.44)
Economic
Poverty: 0.05 (20.13, 0.24) 0.02 (20.10, 0.15) 0.11 (20.08, 0.30) 20.04 (20.15, 0.07)
,200% vs. .=200% (ref)
Education: , high school (HS) 0.33 (0.01, 0.65) 20.08 (20.29, 0.14) 0.74 (0.41, 1.07) 0.11 (20.11, 0.32)
.= HS and ,4 yrs college 0.02 (20.23, 0.27) 20.07 (20.23, 0.08) 0.52 (0.32, 0.71) 0.18 (0.05, 0.30)
.=4 yrs coll (ref) 0.0 0.0 0.0 0.0
Census tract poverty: .=20% 0.13 (20.24, 0.51) 20.02 (20.22, 0.19) 0.20 (20.10, 0.49) 0.06 (20.10, 0.23)
.=5% and ,20% 0.07 (20.31, 0.44) 20.06 (20.28, 0.16) 20.00 (20.26, 0.25) 0.01 (20.13, 0.15)
,5% (ref) 0.0 0.0 0.0 0.0
Parents/guardians
highest education: ,HS
0.33 (0.00, 0.65) 0.09 (20.13, 0.32) 0.28 (20.09, 0.66) 0.01 (20.18, 0.21)
.= HS and ,4 yrs college 20.04 (20.38, 0.30) 0.04 (20.12, 0.21) 0.21 (20.03, 0.44) 0.06 (20.06, 0.18)
.=4 yrs coll (ref) 0.0 0.0 0.0 0.0
Note: Parameter estimates whose 95% CI exclude 0 are indicated in bold highlight. Multivariable analyses controlled for all variables listed in the above columns and
also: response to unfair treatment; social desirability; body mass index; waist to hip ratio; cigarette smoking (current and smoked within 8 hrs of exam, current did not
smoke within 8 hrs of exam; ex-smoker, never smoker); alcohol within 8 hrs of exam (yes; no); food within 8 hrs of exam (yes; no); taking anti-hypertensive medication
(yes; no).
9.9% had less than a high school education, 20% of each group
nevertheless had household incomes over 400% of the US poverty
line, and 15.5% and 33.6% had 4 or more years of college. Of
note, and as shown in Figure 2, whereas the poverty and education
levels of the black participants were on par with or worse than
those of the 2010 black population in Boston and the US [5153],
the white participants, by contrast, were 2 to 3 times more likely to
be currently impoverished compared to the 2010 white non-
Hispanic population in Boston and the US [5153] and half as
likely as Bostons 2010 white non-Hispanic population to have
completed 4 years of college [53].
Also of note, and also shown in Figure 2, the self-report and
implicit measures of racial discrimination, were, for the black
participants, in the lower range, and, for the white participants, in
the higher range, compared to what has been reported in prior
research, especially in relation to studies whose participants had
higher income or education [26,27,54,55]. Thus, the values for the
explicit and implicit measures of racial discrimination among the
black participants were similar to those of other economically
deprived black populations [22,26], but lower than those of black
populations with higher education [27,54]. By contrast, as
compared to other low-income white populations, the white
participants had higher values for the explicit racial discrimination
measures [22,55] and lower values for the IAT/black vs. white
[26].
Perhaps most germane to interpreting results, both the black
and white participants had health profiles considerably worse than
their Boston and US counterparts (Figure 2). For example, the
proportion of black and white MBMS participants who were
current smokers, obese and hypertensive was, contrary to what we
expected, 1.5 to 2 times higher compared to population-based
estimates for Boston and nationally [51,52,56]. These comparative
data thus suggest that the community health center members
from whom the MBMS participants were randomly selected,
without regard to their health status or health care utilization were
disproportionately in poorer health compared to other persons in
the same income range.
Interpretation of results
Our effectively null results regarding associations between
exposure to racial discrimination and risk of cardiovascular disease
among black Americans are not an unusual finding. A 2003 review
article that reviewed 17 US studies published between 1972 and
2001 observed that The existing data on the relationship of
racism to BP [blood pressure] level or HT [hypertension] status
are mixed and concluded that methodological limitations limit
their interpretability and are likely to account for the inconsistent
and relatively weak findings (see [57], p. 62). Of note, similar
summary comments can be found in a series of 3 review articles
published between 2011 and 2013 focused on racial discrimination
and CVD. Thus, a 2011 review article that analyzed 24 US studies
published between 1984 and 2010 concluded: Direct evidence
linking individual/interpersonal racism to [hypertension] HTN
diagnosis is weak but, suggesting that acute rather than chronic
effects may be more readily observed, further stated the
relationship of individual/interpersonal racism to ambulatory
blood pressure (ABP) is more consistent, with all published studies
reporting a positive relationship of interpersonal racism to ABP
(see [4], p. 518). A 2012 review article that critically assessed 15
studies of African Americans published between 1990 and 2012
likewise averred that although its systematic review supports the
association of racial discrimination with an increased risk of
developing hypertension; however, the picture is not uniform and
argued that [m]ethodological challenges, such as floor or ceiling
effects of reported discrimination and low sample size, may have
prevented researchers from detecting important associations (see
[5], p. 422). Another review article, also published in 2012, in turn
focused on 22 US articles on racial discrimination and cardiovas-
Table 6. Black vs. white difference: effect of adjusting for racial discrimination (RD)
a
and socioeconomic position (SEP)
b
, separately
and jointly (imputed data).
CVD outcome
Parameter estimate:
for black vs. white
Model 1 Model 2 Model 3 Model 4
adjusting for: (age + gender) (RD
a
+ core
c
) (SEP
b
+ core
c
) (RD
a
+ SEP
b
+ core
c
)
SBP b (95% CI) 3.79 (1.81, 5.78) 3.77 (0.23, 7.30) 3.81 (1.63, 5.98) 3.80 (0.12, 7.48)
Hypertension OR (95% CI) 2.40 (1.77, 3.24) 2.96 (1.72, 5.12) 2.14 (1.55, 2.97) 2.70 (1.53, 4.75)
Framingham 10 year
CVD risk score
(log-transformed values)
b (95% CI) 20.02 (20.10, 0.06) 0.04 (20.10, 0.18) 20.06 (20.14, 0.03) 20.00 (20.15, 0.14)
Model adjusts for:
age + gender 3 3 3 3
racial discrimination
a
3 3
socioeconomic position
b
3 3
core covariates
c
3 3 3
Note: models run (on the imputed data) for the total study population (504 black and 501 white participants), except for analyses for uncontrolled hypertension, which
were restricted to participants with hypertension (315 black, 209 white); for estimating the black vs. white risk of the outcome, b = parameter estimate for linear
regression, OR = odds ratio for logistic regression, CI = confidence interval; bold italic: 95% CI for b excludes 1 or 95% CI for OR excludes 1. Values for the Framingham
scores are log transformed.
a
RD models: included interaction terms between race/ethnicity and each RD measure (explicit: EOD; implicit: IAT/black vs. white, IAT/me vs. them, and their
interaction; structural: Jim Crow birthplace status); because none of the interaction terms were statistically significant, we report only the main effect.
b
Socioeconomic position: poverty, educational level (participant and participants parents/guardians).
c
Core covariates: age; gender; socioeconomic position (poverty level: household and census tract, education: respondent and highest level attained by parents/
guardians); psychosocial (response to unfair treatment, social desirability); anthropometric (body mass index, waist-to-hip ratio); health behavior (smoking status;
cigarette, food, or alcohol within 8 hrs of exam); for SPB only: taking anti-hypertensive medication.
cular disease published between 2000 and 2010 and reported that,
among 50 tests for associations performed, 40% were null, 30%
revealed global positive associations, of which 67% were
statistically significant, and 15% were negative (i.e., higher
exposure to racial discrimination associated with lower blood
pressure/hypertension) (see [6], p. 956). Thus, conclusive
evidence of either a positive or null association remains elusive.
To this mixed literature, our study contributes two methodo-
logical refinements potentially relevant to future research i.e., the
use of the IAT and the structural measure of racial discrimination.
Moreover, even though our findings are not in accord with our a
priori hypotheses, we do not deem these effectively null findings to
be conclusive. Rather, in light of the above evidence we present on
study participant characteristics, we argue instead that our finding
of weak or no associations between risk of CVD and both the
racial discrimination and socioeconomic measures likely reflects
the unexpectedly poor health profiles of the MBMS participants,
as well as the high levels of lifetime socioeconomic adversity
among both the black and white participants. The net impact, we
argue, was to constrain variability, especially in the outcomes but
also the exposures, thereby limiting our ability to detect the
expected socioeconomic gradient in the CVD outcomes and
hypothesized associations between exposure to racial discrimina-
tion and the CVD outcomes, were such underlying causal
relationships to exist.
In brief, null findings can occur for two very different reasons
above and beyond such well-established reasons as non-differential
or differential measurement error, variables wrongly omitted from
or included in the analytic models, or inadequate sample size
[58,59]. The first is that the hypothesis can be correct, but the
postulated association is not observable in the examined study
population [6063]; for example, as famously observed by
Geoffrey Rose [60], if everyone smokes, no association will be
detected between smoking and lung cancer, despite their causal
connection. The second is that the hypothesis is incorrect, such
that the association would not be observed even with the ideal data
set [6063]. Determining which explanation is most plausible
consequently requires careful scrutiny of study participants range
of exposures and outcomes [6063].
In the case of our study, given plausible theorized pathways by
which racial discrimination and its social and economic conse-
quences can become embodied and harm cardiovascular health
(e.g., direct physiological damage due to chronic activation of
stress responses; health-harming behavioral responses, e.g., smok-
ing; adverse social and biophysical exposures associated with
residential and occupational segregation and material deprivation;
and inadequate medical care) [110], we suggest two lines of
evidence support our interpretation of our null findings. The first
and most important is that we observed unexpectedly small
socioeconomic and racial/ethnic differences in risk for the study
outcomes, despite a large body of population-based research
documenting substantial socioeconomic and racial/ethnic (and
especially US black vs. white) inequities in cardiovascular
mortality, disease, and risk factors [46,64,65]. Additionally, the
two psychometrically-validated explicit racial discrimination mea-
sures we used have been associated in many studies of more
Figure 2. Distributions of average exposure to racial discrimination, socioeconomic position, and cardiovascular risk factors and
outcomes, for My Body My Story participants (20082010) compared to analogous Boston data and US national data.
doi:10.1371/journal.pone.0077174.g002
economically diverse populations with risk of diverse health
outcomes, including CVD risk factors [1,3,46,66]. The combi-
nation of the unexpectedly poor health status of both the black and
white participants, along with recruiting participants during the
20082010 economic recession (perhaps linked to the poorer
socioeconomic profile of the white participants compared to
populations in Boston, the US, and other studies and their use of
community health centers), could thus conceivably account for not
only the null findings vis a vis racial discrimination and the
selected health outcomes, but also lack of a black excess risk for the
Framingham CVD 10 year risk score and also the lack of impact
of controlling for socioeconomic position on the observed black
excess risk for SBP and hypertension.
Ascertaining whether or not the novel implicit and structural
measures we employed accurately capture the relevant exposures,
however, will require more empirical investigation, given the
paucity of analogous research. Of note, the IAT methodology itself
has been extensively validated [25,67,68], and we have shown that
the novel IAT measures we have developed are immune, as
expected, to social desirability (i.e., saying what one thinks is the
expected right answer, as opposed to what one believes
[11,25,69]), whereas lower self-reports of racial discrimination
were strongly associated with higher social desirability [11]. Also
suggesting the Jim Crow measure may have promise, the handful
of extant epidemiologic studies [7074] on the health impact of
Jim Crow indicate its abolition was associated with declines in
infant mortality and preventable mortality among adults, with
likely intergenerational effects [7]. Underscoring the measures
potential importance, in 2013 all US-born persons whose birth
year was in or preceded 1964, i.e., age 47 and older, were born
when Jim Crow was legal with the implication that their parents
and grandparents, if also US-born, were likewise exposed,
depending on their race/ethnicity, to the discrimination or
benefits conferred by Jim Crow [1,7,74]. Suggesting too that
further work is needed to understand the strength and limitations
of the explicit measures we used [20,24], ours is not the first study
to find an effect for one explicit measure not detected with another
measure; new results from the Jackson Heart Study (4939 African
American participants, ages 3584), for example, found a weak
positive association between hypertension and lifetime racial
discrimination (as measured by the EOD; OR =1.08 (95% CI
1.02, 1.15), comparing the highest vs. lowest quartile, adjusted for
age and gender), but no associations with the EDS [75].
No published studies, moreover, have investigated associations
between racial discrimination and the Framingham CVD 10-year
risk score, even as US investigations have documented socioeco-
nomic and racial/ethnic (including black vs. white) disparities in
this and related Framingham risk scores [76]. Although validated
for use across diverse US racial/ethnic groups [12], concerns exist
as to whether these scores may underpredict risk of adverse CVD
outcomes among persons subjected to economic deprivation [64].
Keeping this caveat in mind (which would lead to conservative
estimates of effect), integrated measures of CVD risk (whether the
Framingham scores or analogous measures [12,13,77]) could
nevertheless be useful, precisely because they provide a clinically-
relevant global estimate of risk that takes into account the varying
levels of the specified key risk factors [12,13,77].
In summary, results of our study underscore why appraisal of
findings on racial discrimination and health, and by extension any
exposure-outcome association, requires careful contextualization
of study participants and their range of exposures and outcomes
[1,7]. If our interpretation is correct, it has important implications
for research on health inequities, with regard to clarifying
circumstances in which associations arising from causal relation-
ships, if extant, may or may not be observed.
Supporting Information
Table S1 Univariate and multivariable associations of
racial discrimination, socioeconomic position, and
additional covariates with cardiovascular outcomes:
My Body My Story study (504 black, 501 white US born
non-Hispanic participants; Boston, 20092010) (imputed
data).
(DOCX)
Acknowledgments
We thank, with written permission, the following contributing non-authors
for their contributions to the My Body, My Story study: Beverly Russell, for
helping to establish connections with the community health centers, and
Kristin Mikolowsky, Rachel Rifkin, and Latrice Samuel for recruiting
participants and conducting the interviews. We additionally gratefully
acknowledge, with written permission, the contributions of the following
persons whose contributions made this study feasible: (a) our two short-
term study interviewers: Suzanne Mac Rae and Valerie Polletta; and (b)
staff of the four participating community health centers: (1) Harbor Health
Services (Geiger-Gibson and Neponset): Robert A. Hoch, MD, Corporate
Medical Director, Harbor Health Services, and Joanne Tuller, Psy.D.,
QAI Data Manager, Harbor Health Services; (2) Southern Jamaica Plain
Health Center: Tom Kieffer, MD, PA-C, Executive Director, Michael
Lambert, MD, Medical Director, and Marisol Lara, Medical Unit
Coordinator; (3) Mattapan Community Health Center: Azzie Young,
PhD, MPA, President and CEO, and Sharon T. Callender, RN, MPH,
Coordinator, Family & Community Health Services; and (4) Whittier
Street Health Center: Frederica M. Williams, MD, President & CEO,
Mark Drews, MD, Medical Director, Dalton Skerritt, Program Manager,
Mens Health Program, and Halima Mohamed, MPH, Director of QA &
PI.
Author Contributions
Conceived and designed the experiments: NK PDW AK JTC KWS DRC
GGB DRW GT ERF. Performed the experiments: NK PDW AK DRC.
Analyzed the data: NK PDW AK JTC DRC. Wrote the paper: NK PDW
AK JTC KWS DRC GGB DRW GT ERF. Facilitated work with the
community health centers: ERF GT.
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